Embodiments of the present invention generally relate to neurostimulation systems and methods, and more particularly to restoring sinus rhythm through control of a neurostimulation configuration.
Neurostimulation systems (NS) are devices that generate electrical pulses and deliver the pulses to nerve tissue to treat a variety of disorders. Spinal cord stimulation (SCS) is the most common type of neurostimulation. In SOS, electrical pulses are delivered to nerve tissue in the spine typically for the purpose of chronic pain control. While a precise understanding of the interaction between the applied electrical energy and the nervous tissue is not fully appreciated, it is known that application of an electrical field to spinal nervous tissue can effectively mask certain types of pain transmitted from regions of the body associated with the stimulated nerve tissue. Applying electrical energy to the spinal cord associated with regions of the body afflicted with chronic pain can induce “paresthesia” (a subjective sensation of numbness or tingling) in the afflicted bodily regions. Thereby, paresthesia can effectively mask the transmission of non-acute pain sensations to the brain.
NS and SCS systems generally include a pulse generator and one or more leads. A stimulation lead includes a lead body of insulative material that encloses wire conductors. The distal end of the stimulation lead includes multiple electrodes that are electrically coupled to the wire conductors. The proximal end of the lead body includes multiple terminals, which are also electrically coupled to the wire conductors that are adapted to receive electrical pulses. The distal end of a respective stimulation lead is implanted within the epidural space to deliver the electrical pulses to the appropriate nerve tissue within the spinal cord that corresponds to the dermatome(s) in which the patient experiences chronic pain. The stimulation leads are then tunneled to another location within the patient's body to be electrically connected with a pulse generator or, alternatively, to an “extension.”
The pulse generator is typically implanted within a subcutaneous pocket created during the implantation procedure. In NS, the subcutaneous pocket is typically disposed in a lower back region, although subclavicular implantations and lower abdominal implantations are commonly employed for other types of neuromodulation therapies.
The pulse generator is typically implemented using a metallic housing that encloses circuitry for generating the electrical pulses, control circuitry, communication circuitry, a rechargeable battery, etc. The pulse generating circuitry is coupled to one or more stimulation leads through electrical connections provided in a “header” of the pulse generator. Specifically, feedthrough wires typically exit the metallic housing and enter into a header structure of a moldable material. Within the header structure, the feedthrough wires are electrically coupled to annular electrical connectors. The header structure holds the annular connectors in a fixed arrangement that corresponds to the arrangement of terminals on a stimulation lead.
Spinal cord stimulation is commonly used to treat neuropathic pain. More recently, spinal cord stimulation has been considered as a treatment for various cardiac management applications. These may include angina, heart failure (HF), as well as bradycardia and atrial and ventricular tachyarrhythmias including atrial fibrillation (AF).
Literature has discussed the potential to use SCS to suppress bradycardia and tachycardia. Increasing extrinsic neuronal inputs to the intrinsic cardiac nervous system can initiate self-termination of episodes of atrial tachyarrhythmia (AT) and/or fibrillation (AF) in intact hearts without the need for concomitant programmed electrical stimulation of atrial muscle. However, the proposed electronic and physiologic mechanism to utilize SCS therapy to terminate AF or AT is a complex interaction of sympatholytic and vagotonic signaling. For example, the physiologic mechanism may include both inhibition of sympathetic outflow to the heart and stimulation of afferent fibers that trigger centrally-mediated parasympathetic reflex. However, thus far, no detailed models have been accepted as a complete and accurate description of the interaction of sympatholytic and vagotonic signaling. Hence, it is not yet known what types of NS configurations will yield a desired result for patients experiencing AF or AT.